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25.6.11

The Omega -6-to -Omega -3 Ratio

An often-cited animal experiment suggested that the ideal ratio of omega-6 linoleic acid to omega-3 ALA is four-to-one, but this experiment injected rats with free fatty acids rather than feeding them dietary oils.47 A more realistic experiment that fed rats a mix of various vegetable oils in a broad range of different proportions showed that a ratio of nine-to-one maximized tissue DHA content just as well as lower ratios.48 The precise ratio is likely to be of much less importance, however, when there is preformed arachidonic acid and DHA in the diet. Nevertheless, people who consume the standard American diet rich in vegetable oils may face adverse consequences from consuming excess linoleic acid and people who consume large amounts of fatty fish, fish oil or cod liver oil may face adverse consequences from consuming an excess of the omega-3 fatty acid eicosapentaenoic acid (EPA).
Among ten populations studied from five different continents, American adults have the highest blood levels of omega-6 fatty acids and American infants have the lowest blood levels of omega-3 fatty acids.33 Up until the 1930s, Americans consumed on average about 15 grams (one tablespoon) of PUFA per day. Since the 1930s, this value has more than doubled to over 35 grams per day as Americans have increased their intake of vegetable oils rich in the omega-6 linoleic acid (see Figure 2).2 Most of this increase occurred after 1961 when the American Heart Association began recommending that people replace saturated fats with vegetable oils in order to lower cholesterol levels.3
Similar increases in linoleic acid have been shown to decrease the conversion of ALA to longer-chain omega-3 fatty acids such as DHA in humans.49 Human studies tend to look at the fatty acids incorporated into red blood cells, but animal experiments provide much more detailed information about the concentrations of fatty acids in the organs and glands where they are most needed. These experiments show that excesses of linoleic acid do not increase tissue concentrations of arachidonic acid; instead, they replace the true omega-3 DHA with a “fake” omega-6 version of DHA that ordinarily is not found in substantial amounts within the body.50 The main effect of the excess linoleic acid in the standard American diet is thus most likely to be a mild form of DHA deficiency.
The effect of excess linoleic acid is probably most detrimental to infants and young children whose brains are still developing. DHA deficiency during early development may have lasting effects on cognitive and visual function during adulthood. Animal experiments even suggest that these effects are multi-generational, with the DHA concentration of nervous tissue declining with each successive generation.
Even in adulthood, however, dietary fats influence the DHA concentrations of most other tissues. Recent research has shown that our tissues use DHA to synthesize compounds called “resolvins,” which are involved in bringing inflammatory responses to an end when they are no longer needed.51 Sufficient DHA thus allows the immune system to mount a robust inflammatory response against invading pathogens or damaged tissues and to bring the response quickly to an end once the task has been accomplished. Researchers are increasingly discovering that most degenerative diseases involve an element of chronic, low-level inflammation, and the inability to “turn off” important inflammatory processes once they are no longer needed could be part of the problem. DHA deficiency may therefore be at the root of widespread declines in cognitive function, increases in mental disorders and epidemic levels of degenerative disease.
EPA, a precursor to DHA, is an omega-3 fatty acid that accumulates in fish but generally exists in only infinitesimal quantities in mammals and other land animals. Many authors consider EPA an “anti-inflammatory” essential fatty acid, but its “anti-inflammatory” activity is a result of its ability to interfere with arachidonic acid metabolism. The conversion of arachidonic acid to PGE2 in immune cells is an important initiator of inflammation, but it also turns on the genes necessary for the synthesis of compounds that resolve inflammation, some of which are derived from arachidonic acid and others of which are derived from DHA.52 Providing sufficient DHA to allow the synthesis of the full spectrum of inflammation-resolving compounds is a nutritional approach to inflammation. Providing high doses of EPA that interfere with arachidonic acid metabolism, however, is a pharmacological approach, and it is likely to have many adverse consequences.
When Holman and Widmer first discovered the dichotomy between omega-3 and omega-6 fatty acids, they examined nine different tissues in rats on normal lab diets and could not find even a trace of EPA unless they had first induced essential fatty acid deficiency and all its related tissue damage.32 Several years later Holman conducted a study with another colleague showing that ALA aggravated essential fatty acid deficiency; if they gave the animals vitamin B6, however, the rats converted ALA to DHA rather than to EPA and the aggravating effect disappeared.19 More recent studies in humans have provided preliminary evidence suggesting that EPA interferes with growth in infants and immune function in adults, while DHA improves both growth and immune function.53-54Figure 2. Increase in American PUFA Consumption
Consumption of polyunsaturated fat in
the United States between 1909 and
2005 based on USDA food disappearance
data. From reference 2,
courtesy of Stephan Guyenet’s Whole
Health Source blog
(used with permission).
John Hughes Bennett, a nineteenth century Scottish physician who traveled the world studying the use of cod liver oil in medicine, wrote in his Treatise on Cod Liver Oil that excessive doses over extended periods of time could cause gastrointestinal problems, excessive menstrual bleeding, itchy skin eruptions and excessive evaporation of water through the skin.55 The last three symptoms seem very much like the hormonal disruptions, hemorrhaging and skin problems known to occur during arachidonic acid deficiency. Had the Burrs looked for gastrointestinal disorders during essential fatty acid deficiency, they probably would have found them. Non-steroidal anti-inflammatory drugs (NSAIDs) work their magic by interfering with the production of PGE2 from arachidonic acid, a characteristic they share with EPA. One of the most common set of side effects associated with these drugs is gastrointestinal disturbances. Four out of ten users of NSAIDs experience symptoms such as heartburn, acid reflux, stomach burning, nausea, or bloating.56 Researchers have used NSAIDs to produce food intolerances in mice that result in a form of severe intestinal damage called villous atrophy that is usually associated with celiac disease,57 suggesting that a deficiency of arachidonic acid or the PGE2 made from it may underlie celiac disease and other food intolerances, perhaps by preventing the gut from forming cellular junctions and thus impairing its integrity. Excessive doses of EPA from fatty fish, fish oil and cod liver oil may contribute to all of these symptoms in susceptible individuals.
Our bodies use the same enzymes to convert EPA to DHA as they use to convert ALA to DHA or linoleic acid to arachidonic acid. The same conditions that reduce the requirement for arachidonic acid and DHA are likely to increase a person’s tolerance for EPA. A diet that excludes refined sugar and rancid vegetable oil, is low in total PUFA content, is adequate in protein and total energy, and is rich in vitamin B6, biotin, calcium, magnesium, and fresh, whole foods abundant in natural antioxidants should not carry any risk of arachidonic acid deficiency when moderate amounts of EPA are consumed. Liberal amounts of egg yolks and liver providing preformed arachidonic acid would provide extra insurance against damage by EPA. Under these conditions, it would be safe to consume cod liver oil—valuable for its abundant provision of DHA, vitamin A and vitamin D—in spite of its EPA content.